1. Field of the Invention
The present invention is broadly concerned with a method of preventing or minimizing shedding of Toxoplasma oocysts by cats in their fecal elimination processes and thereby reducing the contamination of soils around human habitations. More particularly, it is concerned with such a method which can be begun after the cat has been subjected to infection, i.e., after the cat has eaten meat (e.g., a wild bird or mouse) which carries Toxoplasma cysts or related forms.
2. Description of the Prior Art
Cats and people are biologically close enough for them to be able to suffer from some of the same diseases and parasites. Some of these ailments are well known--rabies, because it is so dramatic and terrible, and fleas, because they are so common, are two familiar examples. Less familiar is Toxoplasmosis, an animal disease that can be transmitted to man. It is common to all domestic animals, including barnyard species, and, when present, travels through cat feces and through meat.
Any direct contact with cat feces or fecally contaminated soil increases the likelihood of contagion. Cattle and sheep can become infected by ingesting contaminated soil while grazing. Birds may become infected when eating seeds on the ground or from eating contaminated earthworms. However, a domestic cat, after stalking a mouse or bird, may become a disseminator of the disease. Although infected animals may be means of transmitting disease, more often than not there is no sign of illness.
Toxoplasmosis is a parasitic disease, and research has indicated that the parasite has a complicated life cycle which spreads the disease through many animals. Oocysts (egg spores) are shed in the feces of domestic cats and certain types of wild cats. Oocysts are then deposited in soil where they persist for many months. Flies and cokroaches, which eat feces, can serve as transport agents, contaminating animals which do not directly encounter the cat feces or contaminated soil. Mice and birds can be infected either from transport agents or through direct contact or contaminated soil and can then spread the infection to animals which prey on them. Humans can be infected by eating raw or rare meats, or by direct contact with infected cat feces or contaminated soil.
Toxoplasma infections are quite prevalent, with one-quarter to one-half of the adults in the United States and elsewhere asymptomatically infected. While the presence of Toxoplasma infections has long been known, little was discovered about the transmission of Toxoplasma until the late 1930's and 1940's when Toxoplasma was found in newborn babies in the U.S. However, the life cycle of toxoplasma, and the central role played therein by cats, has now been conclusively established.
The spectrum of human disease due to Toxoplasma was characterized by a combination of serologic, immunologic and epidemiological studies, and by isolation of Toxoplasma. In the acute infection where cells are destroyed by rapidly proliferating organisms, there may occur fever, pneumonia, an inflammation in the heart muscle, liver and skin (rash). Toward the end of this period or following a subclinical acute infection, localized or generalized swelling of lymph nodes is observed, especially in women. In newborns infected in utero, a subacute disease picture is typical. In addition to the symptoms of acute Toxoplasmosis mentioned above, meningoencephalitis ("brain fever"), often with hydrocephalus ("water on the brain"), and retinochoroiditis (intraocular inflammation) are important. Most of the mothers who have given birth to infected babies had asymptomatic infections.
Thus, Toxoplasmosis deserves special attention because of the serious danger it raises for the unborn human baby. A pregnant woman may contract the infection and unknowingly infect the fetus. Even if diagnosed and treated, her child may nevertheless be born with permanent brain and eye damage. Surveillance of pregnant women for diagnosis and eventual treatment would be a difficult and costly process. For this reason, efforts to prevent infection during pregnancy are most important.
Inasmuch as cats shed Toxoplasma oocysts after a prepatent (incubation) period of three to ten days after ingestion of cysts in infected animal tissues, it is especially important that such oocyst shedding be controlled or preferably eliminated. That is to say, a normal domestic house cat, while being fed a standard cat food or other ration, may, at infrequent intervals, hunt and eat raw meat such as wild birds and mice, and thereby become infected. The problem, of course, is that it is very difficult to completely control a cat's diet, particularly in cases where the cat has substantial outdoor freedom. A further complication noted above is the fact that primary Toxoplasma infection of cats, during which infectious oocysts are shed, is usually inapparent. Consequently, the soil of yards and gardens close to human habitation can be contaminated with oocysts without raising the suspicion of even an observant cat owner. Such infectious oocysts tend to remain active for a period of months up to a year and a half, thereby presenting a significant health hazard for pregnant women and young children.
Prior attempts to control oocyst shedding were not highly satisfactory. Attempts have been made to administer sulfadiazine alone or with pyrimethamine to cats starting five days after the infectious meal, thereby reducing the number of shed oocysts but not preventing shedding. Pyrimethamine and sulfadiazine have been administered by intramuscular injection; however, when given by mouth these compounds were less effective. Also, the potential toxicity of these drugs suggested the need for blood counts or the administration of antagonists, which is both expensive and time consuming. Other workers have administered a sulfone, sulfadiazine, pyrimethamine, and Clindamycin to cats between two days before to three to four days after infection with Toxoplasma; this served to diminish the shedding in the case of some cats, but did not consistently eliminate this objectionable result.
A number of polyether ionophores are active against coccidia of Eimeria species in chicken and cattle, such as lasalocid, monensin, and salinomycin. However, prior workers administering lasalocid at 5-10 mg./kg./day in two divided doses, mixed with canned cat food, starting the day before infection and continuing for fourteen days, prevented oocyst shedding in only three of nine cats. In short, while the objective of preventing oocyst shedding in infected cats has been studied by others, there is a decided need in the art for a method of preventing such shedding, particularly in the case of domestic cats that obtain a substantial part of their food at home, but that hunt when they escape or are let out of the house.